Poisoning: emergency management

In the case of suspected or definite poisoning, once the patient’s vital parameters have been evaluated and it has been ascertained that the animal is not at risk of imminent death, a careful history should be taken. The information collected must include:

• the onset and progression of the signs;
• signs in other animals living with the affected one;
• use and access to toxic substances, mentioning them (e.g., pesticides, herbicides, antiparasitic products, rat poisons, paints, solvents, drugs and products for domestic use);
• presence of ornamental plants;
• time from the poisoning to the animal’s reception;
• ongoing treatment for previously diagnosed disorders.

If the animal’s owner knows which poison the patient has been exposed to, she or he should be asked to produce the poison so that the composition and concentration can be determined; with this information an attempt should be made to calculate the amount assumed. The packaging of a toxic substance may also be useful because the manufacturer should indicate the concentration, routes of exposure to the toxic compound and any antidotes.

EVALUATION OF THE POISONED PATIENT

On reception of an intoxicated or poisoned animal, the patient’s vital signs should be monitored and recorded in the following chronological order:

1. airway patency;
2. breathing: type and frequency;
3. cardiovascular system: heart rate, characteristics of the pulse, mucosal colour, capillary filling time;
4.  state of consciousness and any neurological symptoms;
5. body temperature.

Airways. Patients that lose consciousness or have neuromuscular paralysis/paresis or respiratory distress may need orotracheal intubation and positive pressure ventilation. Intubation is also necessary when gastric lavage is performed. When hypoxaemia is present, the animal must be given oxygen, while in cases of respiratory distress with hypercapnia, ventilation must be supported with appropriate procedures.

Cardiovascular system. An adequate availability of oxygen depends on cardiac output, volume of circulating blood and the total content of oxygen in the blood. For this reason, in patients with poor perfusion, effective circulation must be restored through fluid therapy and, if considered appropriate, also through the administration of vasoactive amines. An electrocardiographic evaluation must be carried out if arrhythmias are suspected, if abnormalities of the pulse are present, or if abnormal heart sounds are detected by cardiac auscultation. Some poisonous plants, such as the oleander, are toxic to the heart and it is, therefore, worth checking whether the toxicity of plants also includes cardiotoxicity. Some toxins affect the smooth muscle of vessel walls directly while others damage the vascular endothelium; for this reason it is always useful to measure the affected animal’s blood pressure. When hypertension is detected (systolic blood pressure >160 mmHg) it may be necessary to administer drugs that lower blood pressure, such as amlodipine 0.1-0.4 mg/kg s.i.d. per os or, in severe cases, use direct vasodilators, such as hydralazine (in cats: 1.0-2.5 mg/cat s.c. or 2.5-10 mg every 12 hours per os; in dogs: 0.5-3 mg/kg every 8-12 hours per os starting with the lower dose and up-titrating the dose in relation to the effect of the drug) or sodium nitroprusside (at a dose of 0.5-1 mg/kg/min i.v. by  constant rate infusion). The blood pressure must be monitored when vasoactive drugs are used; the appearance of tachycardia, pale mucosae, cold extremities and a prolonged capillary filling time may indicate an inadequate circulating volume, cardiogenic or hypovolaemic shock.

Neurological signs. Patients with convulsions or severe tremors of skeletal muscles must be treated quickly. The first treatment may be a benzodiazepine such as diazepam or midazolam; the former is administered at a dose of 0.5-1 mg/kg by i.v. bolus. Patients receiving chronic treatment with phenobarbital may need higher doses (2 mg/kg i.v.) because of the increased hepatic metabolism induced by long-term administration of barbiturates. The dose of midazolam is 0.3-0.5 mg/kg as an i.m. or i.v. bolus; since midazolam is prepared in an aqueous vehicle, it can also be administered intramuscularly. Its duration of action is shorter than that of diazepam, but it has a greater muscle relaxant effect and can, therefore, be very useful in controlling muscle spasms in patients with convulsions and thus enabling the creation of a venous access. Midazolam acts equally quickly after intramuscular or intravascular administration. When a venous access is not available, diazepam can be given intranasally or rectally at a dose of 1-2 mg/kg, or by the intramuscular route: in this last case, the intravenous dose is used. In patients that respond positively to benzodiazepines, which are short-acting drugs, a continuous infusion can be given: diazepam 0.5-2 mg/kg/hour i.v. or midazolam 0.05-0.3 mg/kg/hour i.v.

When diazepam does not control the convulsions, barbiturates, such as phenobarbital at a dose of 2-6 mg/kg i.m., can be used. Phenobarbital takes 15-20 minutes to start working; if results have not been achieved within 30 minutes of its administration, the dose can be repeated up to a total of 15 mg/kg in 24 hours. Pentobarbital can also be used when benzodiazepines are ineffective: it is administered at a dose of 2-10 mg/kg i.v. to reach the therapeutic effect. It can control convulsions, but should only be used in cases in which the previously mentioned therapies have failed since it can accumulate. Propofol has anticonvulsant properties and does not cause accumulation phenomena in dogs (whereas accumulation can occur in cats after prolonged infusions of this drug); the dose is 1-8 mg/kg i.v. or 0.01-0.25 mg/kg/hour in a constant rate infusion.

Once the patient’s clinical condition has been evaluated, the next steps are:

• to identify any acid-base imbalances and electrolyte disorders and establish a ‘minimum database’ (at least blood glucose, total proteinsand uraemia);
• to carry out decontamination (e.g. gastrointestinal or cutaneous);
• to provide support for vital functions and for specific organs, when necessary.

The direct effects of toxic substances and the consequence of their ingestion, such as vomiting, diarrhoea, convulsions and muscle tremors, can cause life-threatening modifications to the acid-base balance, loss of electrolytes, altered levels of uraemia and, in some cases, organ failure. It is, therefore, recommended that a so-called ‘emergency database’ is always established in the case of poisoning. The database should contain information on the acid-base status and on the levels of the main electrolytes (sodium, potassium, chloride), PCV, total proteins, uraemia and blood glucose. Based on all these data, the targeted fluid therapy can be given without the risk of administering the wrong fluid and, thereby, compromising vital functions or worsening the patient’s condition (e.g. by causing iatrogenic hyponatraemia and alkalosis). The most frequently found acid-base imbalances and mild electrolyte disturbances, such as metabolic acidosis and hypokalaemia, are corrected with maintenance fluid therapy consisting of balanced crystalloid solutions administered intravenously in the first 24 hours; the fluid therapy should, of course, be associated with specific treatment of the aetiological cause and with supportive treatment.

Some patients have mixed acid-base imbalances that are difficult to treat, such as metabolic acidosis due to circulatory failure combined with a respiratory acidosis due to central nervous system depression following the administration of drugs that depress the sensorium (e.g. benzodiazepines and barbiturates). In these cases a missed diagnosis or incomplete quantification of the disorder can result in a poor outcome or prolong the time necessary for the patient’s vital functions to recover. Respiratory acidosis due to hypoventilation is typical of acute poisoning caused by numerous toxins that act on skeletal muscles and on the central nervous system.

Alkalosis due to emesis (as a result of loss of hydrochloric acid from the stomach) is treated with anti-emetics and fluids with an acid pH (0.9% saline solution). Hypoventilation caused by pain or hypoxia produces a respiratory alkalosis that must be treated with aetiologically targeted therapy. Some poisons can directly affect the following parameters, which must always be monitored: blood glucose, calcaemia, kalaemia, natraemia and blood chloride levels. In some cases, however, the changes in these parameters are due to metabolic complications induced by the poisoning (e.g. hypoglycaemia in convulsive crises as a result of depletion of glucose stores) and it is, therefore, good practice to monitor them in all cases of severe poisoning. When acute liver damage is suspected, tests of liver function (e.g. albumin, total bilirubin, bile acids and a coagulation screen) should be carried out in addition to the standard tests for the emergency database.

GASTROINTESTINAL DECONTAMINATION

The purpose of gastrointestinal decontamination is to prevent or decrease the absorption of the toxin. There are three stages:

1. elimination of the toxin from the gastrointestinal tract (induction of vomiting, gastric lavage, intestinal irrigation, enemas);
2. administration of intestinal adsorbents or chelating agents;
3. gastrotomy.

Emesis should be induced if the poison has been assumed within the preceding 1-2 hours. However, in some cases in which the poison has been ingested in the form of capsules or tablets, absorption can be delayed and induction of emesis can, therefore, be useful even after 2 hours have passed since the ingestion. Various different drugs can be used to induce vomiting in cats and dogs: hydrogen peroxide 3% administered per os at a dose of 1-2 ml/kg irritates the gastric mucosa causing vomiting within 10-20 minutes; washing up liquid, at a dose of 10 ml/kg, acts in the same way and induces emesis about 20 minutes after the procedure. The efficacy of these two methods depends in part on the condition of the gastric mucosa; if the animal has recently eaten food containing lipids it may be more difficult to induce vomiting and when it is achieved it may be delayed or only partially effective in removing the poison. Both the aforementioned substances can aggravate lesions of the gastrointestinal tract already damaged by the ingestion of toxic substances. A much more reliable and effective treatment is apomorphine, which acts on chemoreceptors of the trigger zone in the central nervous system. If administered intramuscularly the emetic effect is produced within 5 minutes, if administered intravenously the effect is immediate but the drug can cause cardiac, respiratory and central nervous system depression and prolonged vomiting. The dose of apomorphine in the dog is 0.03 mg/kg i.v., 0.04 mg/kg i.m., 0.08 mg/kg s.c. or 0.3 mg/kg diluted with a sterile preparation and instilled into the conjunctival sac. Side effects can be controlled by the administration of naloxone at a dose of 0.01-0.04 mg/kg i.v.; an excessive emetic effect when the apomorphine has been instilled into the conjunctival sac can be counteracted by rinsing with physiological saline. Xylazine, sometimes used as an emetic in cats at a dose of 0.5-1 mg/kg i.m. or 0.44 mg/kg s.c., causes vomiting within 5-10 min, but can produce hypotension, bradycardia, respiratory depression and profound sedation; the antagonist is  yohimbine 0.1 mg/kg i.v.  Emesis should not be induced if the patient has eaten or drunk a caustic substance (e.g. caustic soda, hydrocarbons) or substances capable of damaging the gastrointestinal mucosa severely, since vomiting the toxin could worsen lesions already present in the oesophagus, larynx and oral cavity.

Gastric lavageis performed when induced vomiting is not effective or when it not possible to induce emesis, for example, in unconscious patients and when the toxic substance damages tissues (e.g. strong acids and bases). In order to carry out gastric lavage the patient must be sedated, intubated and placed in the lateral recumbency. The tube must be as long as the distance between the tip of the nose and the last rib and the length to be introduced must be marked on the tube with a sticking plaster or an indelible pen. The diameter of the tube should be as large as possible and the tips non-traumatic and fenestrated. Stethoscopic auscultation of the area of the stomach following a trial passage of air or water through the tube can be used to check the correct position of the tip of the tube in the stomach; aspiration of fluid or gastric contents also confirms the correct position of the tube. Once the position of the tube has been determined, the patient is placed with the head lower than the rest of the body and 5-10 ml/kg of room temperature physiological saline is introduced through the tube. The gastric contents are then removed by a siphoning technique. The procedure should be repeated about ten times until all the toxic substance has been removed or until the fluid removed from the stomach is clear and does not contain any toxic substances. Once the gastric lavage has been completed, the patient is given 1-2 g/kg of activated charcoal. Aspiration pneumonia is the most common complication (especially if the patient is not intubated): the strategy to prevent this complication is to use an orotracheal tube that is as large as feasible and cuffed. As the tube used for the lavage is removed, it should be bent in order to prevent loss of material from the distal tip in the oesophagus and oral cavity. Other possible complications include laryngospasm, hypoxia, hypercapnia, mechanical damage to the airways, trauma and lacerations of the oesophagus and stomach.

Intestinal irrigation is a procedure used above all in human medicine for eliminating toxic substances from the gastrointestinal tract; it is employed for substances that are absorbed slowly (e.g. copper and lithium) but that are able to adhere to the intestinal mucosa and are released continuously. It is contraindicated in subjects with intestinal perforation, occlusions, gastrointestinal bleeding, uncontrollable vomiting and haemodynamic instability. A balanced electrolyte solution containing polyethylene glycol 6% is given per os; this solution transits throughout the intestines without being absorbed, facilitating the removal of the intestinal contents. The patient must undergo general anaesthesia and be intubated; subsequently 25-40 ml/kg of solution is administered through the naso-oesophageal tube, followed by a continuous infusion of the same solution at the rate of  0.5 ml/kg/hour. The solution may also be administered as boluses of 30-40 ml/kg every 2 hours. The most frequent complications are nausea, vomiting, regurgitation and colic.

Laxatives may be used to increase the velocity of intestinal transit, thereby shortening the time the poison remains in the intestines and limiting its absorption. The efficacy of laxatives is increased when they are combined with activated charcoal because of the adsorbent properties of the latter.

In some cases it can be useful to perform enemas with warm water to remove the poison from the colon (washout enema). The water is infused through the rectum until the colon is dilated (using about 50 ml in cats and from 50 to 2000 ml in dogs depending on the size of the animal). The procedure is repeated until a clear solution, or at least a solution free of toxic substances (e.g. metaldehyde), is obtained. Hypertonic enemas are not recommended because they can cause severe electrolyte disturbances; enemas based on mineral oils can be used, but are less effective.

Intestinal adsorbents inhibit the absorption of toxins in the gastrointestinal tract. The most widely used adsorbent is activated charcoal, given that it is able to adsorb most poisons. It is administered repeatedly, with the purpose of interrupting the enterohepatic circulation of some toxic substances. Its adsorbent surface contains numerous atoms of carbon that bind compounds with different degrees of affinity (preferentially neutral and non-polar molecules) until equilibrium is reached and then subsequently releases them in the lumen of the intestines; for this reason, it is useful to combine intestinal adsorbents with laxatives, thereby shortening the gastrointestinal transit time and the possibility of adsorbed particles being released. The dose of activated charcoal to administer depends on the amount and type of poison ingested and whether there is food present in the stomach, but must be ten times greater than the amount of poison; usually a dose of 1-4 g/kg per os, diluted in water (1 g/5-10 ml water), is given every 6 hours. Mineral oils should not be used with activated charcoal because they reduce its efficacy. Patients should be hydrated at the end of treatment to reduce the risk of dehydration. An alternative to activated charcoal for patients with severe lesions of the gastrointestinal mucosa (e.g. bleeding ulcers) is diosmectite which has adsorbent properties, although it is less effective than activated charcoal. The dose in cats and small dogs is 1-1.5 g per os b.i.d. or t.i.d., while that in large dogs is 3 g per os b.i.d. or t.i.d. In the case of poisoning by acid or corrosive substances, magnesium hydroxide (MgOH) 3-4% can be administered at a dose of 5-30 ml per os s.i.d. or b.i.d. in the dog and 5-15 ml per os s.i.d. or b.i.d. in the cat.

Sodium bicarbonate should not be administered after the ingestion of acids because exothermic reactions could occur, causing severe damage to the gastrointestinal mucosa. Egg whites can be given after the intake of caustic substances (4-6 eggs in 250 ml of warm water); egg white has a demulcent effect. Milk has been used in some circumstances, although it is contraindicated in the case of ingestion of hydrocarbons or other liposoluble substances because it can accelerate their absorption.

When all the methods listed above have failed to remove the poison,  a gastrotomy can be considered for the physical removal of the toxin (e.g. pieces of copper which adhere firmly to gastric or intestinal mucosa).

Following stabilisation of the patient and gastrointestinal decontamination, supportive therapy can be started. The most widely used supportive therapy is the promotion of diuresis with intravenous fluid therapy: this aids the excretion of the toxin and can be useful in cases of suspected but not confirmed poisoning. Fluid therapy with crystalloids must lead to the production of at least 2 ml/kg/hour of urine. Intoxicated patients often develop hypothermia following the poisoning, sedation and treatments performed; body temperature must, therefore, be monitored regularly (every 4-6 hours) until normal thermoregulation has been restored and the hypothermic patient must be warmed with active systems (e.g. hot air) or passive ones (e.g. blankets). Anorexic patients must be encouraged to eat by giving them moist, warm food or, if necessary, appetite stimulants. For example, diazepam can be used in both dogs and cats at a dose of 0.05-0.17 mg/kg i.v.: the effect is immediate and so food should be offered contemporaneously with the benzodiazepine. When the animal does not eat spontaneously, it should be given forced enteral nutrition as early as possible. Poisoned patients must be monitored closely in order to pick up signs of any gastrointestinal, respiratory and neurological complications as promptly as possible.

Suggested reading

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